The endogenous Apc promoter drives expression of a phosphomimetic form of Apc2 (two of the conserved Ser residues in the potential GSK3 phosphorylation site of region B have been mutated to Asp).
The embryonic lethality along with the cuticle defects (loss of denticles, expansion of naked cuticle) characteristic for maternal/zygotic Apc2g10,ApcQ8 mutants is rescued by combination with Apc2DD.